AJP - Renal Physiology, Vol 253, Issue 5 952-F958, Copyright © 1987 by American Physiological Society
Role of AVP in malignant DOC-salt hypertension: studies using vascular and antidiuretic antagonists
J. Filep, J. C. Frolich and E. Foldes-Filep
Department of Physiology, Semmelweis University Medical School, Budapest, Hungary.
To investigate the role of arginine vasopressin (AVP) in the maintenance of
blood pressure in deoxycorticosterone (DOC)-salt hypertension, the effects
of specific pressor and antidiuretic antagonists of AVP were studied in
conscious, freely moving rats with established malignant DOC-salt
hypertension. Plasma AVP level was significantly higher in hypertensive
than in normotensive animals (4.8 +/- 1.0 vs. 2.0 +/- 0.3 fmol/ml, n = 5, P
less than 0.02). Administration of d(CH2)5-d-Leu-VAVP, 10 micrograms/kg, an
AVP antagonist that blocked the antidiuretic, but not the pressor effect of
exogenous AVP, induced diuresis, and caused a transient fall in blood
pressure from 173 +/- 3 to 167 +/- 4 mmHg (n = 8, P less than 0.01) with a
concomitant slight increase in heart rate. Similar changes were observed
after administration of d(CH2)5Tyr(Et)VAVP, 10 micrograms/kg, an
antidiuretic plus pressor antagonist of AVP. Intravenous injection of
d(CH2)5Tyr(Me)AVP, 10 micrograms/kg, a specific AVP pressor antagonist had
no effect on blood pressure or heart rate, although it completely abolished
the pressor response to exogenous AVP. Plasma renin activity remained
suppressed following administration of all AVP antagonists. These findings
suggest that if AVP should contribute to maintaining high blood pressure in
malignant DOC-salt hypertension it would have to be the results of its
antidiuretic and not its vasoconstrictor property.
